IL-23/IL-17 axis in IBD

Abstract

Gut inflammation occurring in patients with Crohn's disease and patients with ulcerative colitis has been traditionally associated with an exaggerated Th1 or Th2 cell response, respectively. However, recent studies have shown that in both inflammatory bowel diseases (IBD) there is also enhanced synthesis of cytokines made by a distinct subset of T helper cells, termed Th17 cells. The discovery that this new T-cell subset drives immune-mediated pathology in the gut, and that interleukin (IL)-23 amplifies Th17 cell responses and gut inflammation, has contributed to elucidate new pathways of tissue damage as well as to open new avenues for development of therapeutic strategies in IBD. Nonetheless, it has been recently shown that Th17-related cytokines, such as IL-17A and IL-22, can exert protective rather than detrimental effects in the gut. We here review the available data regarding the role of Th17 cells and IL-23 in chronic intestinal inflammation.